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首页> 外文期刊>Mechanisms of Development >Asymmetry in Histone H3 variants and lysine methylation between paternal and maternal chromatin of the early mouse zygote
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Asymmetry in Histone H3 variants and lysine methylation between paternal and maternal chromatin of the early mouse zygote

机译:组蛋白H3变体的不对称性和早期小鼠合子的父本​​和母本染色质之间的赖氨酸甲基化

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In mammalian fertilization, the paternal genome is delivered to the secondary oocyte by sperm with protamine compacted DNA, while the maternal genome is arrested in meiotic metaphase II. Thus, at the beginning of fertilization, the two gametic chromatin sets are strikingly different. We elaborate on this contrast by reporting asymmetry for histone H3 type in the pre-S-phase zygote when male chromatin is virtually devoid of histone H3.1/3.2. Localization of the histone H3.3/H4 assembly factor Hira with the paternal chromatin indicates the presence of histone H3.3. In conjunction with this, we performed a systematic immunofluorescence analysis of histone N-tail methylations at position H3K4, H3K9, H3K27 and H4K20 up to the young pronucleus stage and show that asymmetries reported earlier are systematic for virtually all di- and tri-methylations but not for mono-methylation of H3K4 and H4K20, the only marks studied present in the early male pronucleus. For H4K20 the expanding male chromatin is rapidly mono-methylated. This coincides with the formation of maternally derived nucleosomes, a process which is observed as early as sperm chromatin decondensation occurs. Absence of tri-methylated H3K9, tri-methylated H4K20 and presence of loosely anchored HP1-beta combined with the homogenous presence of mono-methylated H4K20 suggests the absence of a division of the paternal chromatin in eu- and heterochromatin. In summary the male, in contrast to female G1 chromatin, is uniform and contains predominantly histone H3.3 as histone H3 variant.
机译:在哺乳动物的受精中,父本基因组通过精蛋白与精蛋白紧密结合的DNA被精子传递至次级卵母细胞,而母本基因组则被阻滞在减数分裂中期II中。因此,在受精开始时,两个配子染色质组显着不同。当雄性染色质实际上缺乏组蛋白H3.1 / 3.2时,我们通过报告前S期合子中组蛋白H3类型的不对称性来阐述这种对比​​。组蛋白H3.3 / H4装配因子Hira与父本染色质的定位表明存在组蛋白H3.3。与此结合,我们对直至年轻前核阶段的H3K4,H3K9,H3K27和H4K20位置的组蛋白N尾甲基化进行了系统的免疫荧光分析,结果表明,较早报道的不对称现象实际上对所有二甲基和三甲基化都是系统性的,但并非针对H3K4和H4K20的单甲基化,研究的唯一标志存在于早期男性前核中。对于H4K20,膨胀的雄性染色质迅速被单甲基化。这与母体来源的核小体的形成相吻合,这种过程最早在精子染色质发生缩聚时观察到。三甲基化的H3K9,三甲基化的H4K20的缺乏和锚固的HP1-β的松散结合以及单甲基化的H4K20的均一的存在提示在正常染色质和异染色质中不存在父系染色质的分裂。总之,与雌性G1染色质相反,雄性是均匀的,并且主要包含组蛋白H3.3作为组蛋白H3变体。

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